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5 and IL-18 in Eosinophil Mediated Pathogenesis of Allergic Diseases T ⁎ Hemanth Kumar Kandikattu, Sathisha Upparahalli Venkateshaiah, Anil Mishra

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5 and IL-18 in Eosinophil Mediated Pathogenesis of Allergic Diseases T ⁎ Hemanth Kumar Kandikattu, Sathisha Upparahalli Venkateshaiah, Anil Mishra Cytokine and Growth Factor Reviews 47 (2019) 83–98 Contents lists available at ScienceDirect Cytokine and Growth Factor Reviews journal homepage: www.elsevier.com/locate/cytogfr Synergy of Interleukin (IL)-5 and IL-18 in eosinophil mediated pathogenesis of allergic diseases T ⁎ Hemanth Kumar Kandikattu, Sathisha Upparahalli Venkateshaiah, Anil Mishra Department of Medicine, Tulane Eosinophilic Disorders Centre (TEDC), Section of Pulmonary Diseases, Tulane University School of Medicine, New Orleans, LA 70112, United States ARTICLE INFO ABSTRACT Keywords: Eosinophils are circulating granulocytes that have pleiotropic effects in response to inflammatory signals in the Allergy body. In response to allergens or pathogens, exposure eosinophils are recruited in various organs that execute Eosinophils pathological immune responses. IL-5 plays a key role in the differentiation, development, and survival of eo- IL-5 sinophils. Eosinophils are involved in a variety of allergic diseases including asthma, dermatitis and various IL-18 gastrointestinal disorders (EGID). IL-5 signal transduction involves JAK-STAT-p38MAPK-NFκB activation and Immune responses executes extracellular matrix remodeling, EMT transition and immune responses in allergic diseases. IL-18 is a Th2 responses classical cytokine also involved in immune responses and has a critical role in inflammasome pathway. We recently identified the IL-18 role in the generation, transformation, and maturation of (CD101+CD274+) pa- thogenic eosinophils. In, addition, several other cytokines like IL-2, IL-4, IL-13, IL-21, and IL-33 also contribute in advancing eosinophils associated immune responses in innate and adaptive immunity. This review discusses with a major focus (1) Eosinophils and its constituents, (2) Role of IL-5 and IL-18 in eosinophils development, transformation, maturation, signal transduction of IL-5 and IL-18, (3) The role of eosinophils in allergic disorders and (4) The role of several other associated cytokines in promoting eosinophils mediated allergic diseases. Abbreviations: 2-CDA, 2-Chlorodeoxyadenosine; AD, atopic dermatitis; AP-1, activator protein 1; AR, allergic rhinitis; APRIL, A proliferation-inducing ligand; ASC, adaptor protein; BCL-XL, B-cell lymphoma-extra large; Btk, Bruton’s tyrosine kinase; C/EBP, CCAAT/enhancer binding protein; CARD, C-terminal caspase-recruit- ment domain; CCL, chemokine (C-C motif) ligand; CCR3, CC-chemokine receptor 3; CD, cluster of differentiation; c-fos, FBJ murine osteosarcoma viral oncogene homolog; c-jun, proto-oncogene; CLC, Charcot-Leyden crystal protein; COPD, chronic obstructive pulmonary disease; CRTH2, Chemoattractant receptor homologous molecule expressed on T helper type 2 cells; CXCL, chemokine (C-X-C motif) ligand; CXCR, CXC chemokine receptor; DAMPs, damage-associated molecular patterns; DC, dendritic cell; EC, Eosinophilic cystitis; ECE, eosinophilic cellulitis; ECO, eosinophilic colitis; ECP, eosinophil cationic protein; EDN, eosinophil-derived neu- rotoxin; EF, eosinophilic fasciitis; EG, eosinophilic gastritis; EGE, eosinophilic gastroenteritis; EGF, epidermal growth factor; EGID, eosinophilic gastrointestinal disorders; EGPA, eosinophilic granulomatosis with polyangiitis; EM, eosinophilic myocarditis; EMT, epithelial-mesenchymal transition; EOE, eosinophilic esopha- gitis; EP, eosinophilic pneumonia; EPX, eosinophil peroxidase; ERK, extracellular signal-regulated kinase; FcεRI, Fc fragment of IgE receptor I; FGF, fibroblast growth factor; FIP1L1-PDGFRA, factor interacting with PAPOLA and CPSF1-like-1–platelet-derived growth factor receptor; FOXP3, forkhead box P3; Gal-10, galectin-10; GATA, globin transcription factor; GI, gastrointestinal; GM-CSF, granulocyte macrophage-colony stimulating factor; GTPase, guanine binding protein Rac1; HES, hypereosinophilic syndrome; hIL-5Rα, human interleukin-5 receptor alpha; HLA‐DRB4, HLA Class II histocompatibility antigen-DR Beta 4 Chain; HS1, hematopoietic lineage cell-specific protein1; ICAM-1, Intercellular adhesion molecule 1; IFN-γ, interferon gamma; IgE, immunoglobulin E; IkB kinase, inhibitor of nuclear factor kappa-B kinase; IL, interleukin; ILC2s, type 2 innate lymphoid cells; iNKT, invariant natural killer T cells; IRAK, interleukin-1 receptor-associated kinase 1; JAK, Janus kinase; JNK, c-Jun N-terminal protein kinase; LFA-1, lymphocyte function-associated antigen 1; MAPK, mitogen-activated protein kinases; MBP, major basic protein; MPO, myeloperoxidase; MyD88, myeloid differentiation primary response 88; NADPH, nicotinamide adenine dinucleotide phosphate; NFκb, nuclear factor kappa B subunit; NK, natural killer; NLRP3, NLR family pyrin domain containing 3; OVA, ovalbumin; p50, nuclear factor kappa-B P50 Subunit; p65, transcription factor p65; PAMPs, pathogen-associated molecular patterns; PDGFRα, platelet-derived growth factor receptor alpha; PE, pulmonary eosinophilia; PI3K, phosphoinositide-3- Kinase; Pim-1, proto-oncogene serine/threonine-protein kinase-1 Pim-1; PKCζ, Protein kinase C zeta; PMN, polymorphonuclear neutrophils; PU.1, transcription factor PU.1; PYD, pyrin domain; Raf-1, Raf-1 proto-oncogene serine/threonine kinase; Ras, retrovirus-associated DNA sequences; rIL-15, recombinant interleukin-15; rMIL-21, recombinant mouse interleukin-15; Shc, Src homology 2 domain containing transforming protein 1; SHP2, protein-tyrosine phosphatase 2C (PTP-2C); SIGLEC, sialic acid binding immunoglobulin-like lectin; SIGLECF, sialic acid binding Ig-like lectin; STAT, signal transducer and activator of transcription; TARC, thymus and activation-regulated chemokine; TFH cell, follicular helper T cells; TGF-β1, transforming growth factor beta 1; Th2, T helper cell type 2; TLR, toll-like receptor; TNF-α, tumor necrosis factor alpha; TRAF6, TNF receptor associated factor 6; TREG cells, regulatory T cells; VEGF, vascular endothelial growth factor ⁎ Corresponding author. E-mail address: [email protected] (A. Mishra). https://doi.org/10.1016/j.cytogfr.2019.05.003 Received 11 February 2019; Received in revised form 28 April 2019; Accepted 9 May 2019 Available online 10 May 2019 1359-6101/ © 2019 Elsevier Ltd. All rights reserved. H.K. Kandikattu, et al. Cytokine and Growth Factor Reviews 47 (2019) 83–98 1. Introduction eosinophils produce Th2 cytokines (IL-4, IL-5, and IL-13). Eosinophils regulate dendritic cells and Th2 pulmonary immune responses [15]. Eosinophils are likely first observed in 1846 by Wharton Jones and Eosinophils suppress Th17 and Th1 responses via DC regulation. Eosi- named by Paul Ehrlich in 1879, with time they have traditionally nophil products can serve as Th2 adjuvants via DC regulation. considered effector cells in the innate immune system. Eosinophils are Eosinophils also regulate T-cell development in the thymus. granulocytic leukocytes that develop in the bone marrow from plur- Eosinophils recognize PAMPs and defense against viral, parasitic and ipotent progenitors and share many features with neutrophils, in- bacterial infection. Eosinophils and mast cells mutually potentiate in cluding growth and development in the bone marrow. In contrast with asthma and eosinophilic esophagitis. Mast cells support the survival and neutrophils, eosinophils exit the bone marrow and reside in the activation of eosinophils by secreting IL-5. Eosinophil MBP activates bloodstream with a half-life of ˜18 h and migrate to the thymus, gas- mast cells and basophils, and release cytokines, histamine, and TNF-α trointestinal tract under homeostatic conditions. Eosinophils arise from [6]. Eosinophils play a key role in tissue destruction and repair. Epi- hematopoietic CD34+ progenitor cells in the bone marrow and are of thelial cells of various tissues stimulate eosinophil secretion of TGF-β 5% of total white blood cells in healthy subjects. Eosinophils are dis- and fibroblast growth factors and play a role in tissue repair and also tinguished phenotypically by their bilobed nuclei and cytoplasmic promote wound healing [16–19]. granules filled with cytotoxic and immunoregulatory proteins [1]. Adipose tissue residential eosinophils regulate local cytokine milieu Mature eosinophils in the blood are less than 400 per mm3. Eosinophils and glucose homeostasis. Eosinophils play a role in adipose tissue respond to signals from cytokines, chemokines, and other proin- macrophage polarization and glucose metabolism critical for main- flammatory mediators via cell-specific receptors most notably by cy- taining adipose tissue M2 macrophages [20]. Human eosinophils pro- tokine interleukin-5 (IL-5) and the eotaxin chemokines. During eosi- moted dorsal root ganglia neuron branching. Peripheral dorsal root nophilopoiesis, eosinophils acquire IL-5Rα and IL-18Rα on the cell ganglia and airway neurons produce eotaxins to chemoattract eosino- surface and differentiate under the influence of both IL-5 and IL-18 [2]. phils [21,22]. Eosinophils producing nerve growth factor and neuro- Transcription factors play a crucial role in eosinophilic lineage com- trophins regulate neuronal activity [23]. Eosinophils in the GI tract play mitment in the bone marrow to maturation and development of eosi- a role in homeostasis and disease contexts, such as in EGID promoting nophils. Eosinophilic progenitors express C/EBPα, C/EBPε, PU.1, and IgA class-switching, enhancing intestinal mucus secretions, determining GATA-1 and GATA-2 [3]. The increased production of eosinophils is intestinal microbiota and inducing the development of Peyer’s patches observed in various allergic conditions, skin diseases, parasitic
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